ENDOVASCULAR TREATMENT OF AVMS - Jefferson TREATMENT OF AVMS Rohan Chitale, PGY III Department of...

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ENDOVASCULAR TREATMENT OF AVMS Rohan Chitale, PGY III Department of Neurosurgery, TJUH Grand Rounds April 2, 2010

Transcript of ENDOVASCULAR TREATMENT OF AVMS - Jefferson TREATMENT OF AVMS Rohan Chitale, PGY III Department of...

ENDOVASCULAR TREATMENT OF AVMSRohan Chitale, PGY III

Department of Neurosurgery, TJUH

Grand Rounds April 2, 2010

Arteriovenous Malformations

Congenital abnormal collection of blood vessels wherein blood flows from arterial circulation directly into venous circulation, bypassing capillary bedsIncidence/Prevalence not definitively studied, but estimated incidence is 1.1/100,000 in population-based studiesSlight male preponderanceAverage age diagnosed ~33 years old

Arteriovenous Malformations

Presentation/Clinical Features

Hemorrhage (50%)Intracerebral, subarachnoid, intraventricular

Seizures (20-25%)Headache (15%)Mass effect - direct compression/swelling of adjacent structuresIschemia - preferential flow through the AVM due to decreased resistance, causing hypoperfusion of surrounding brain parenchyma

Why Treat AVMs

2-4% annual risk of ruptureIndependent risk factors for rupture:

Associated aneurysm (feeding artery, intranidal)Previous ruptureSmall AVM sizeDeep venous drainage

Goal is to determine risk of conservative treatment vs risk of intervention

ARUBA trial – A Randomized Trial of Unruptured Brain AVMs

Spetzler-Martin Classification

SizeSmall (< 3cm) 1Medium (3-6 cm) 2Large (> 6 cm) 3

Eloquence of adjacent brainNon-eloquent 0Eloquent 1

Pattern of venous drainageSuperficial only 0Deep 1

Pretherapeutic Evaluation

Noninvasive TechniquesCT/CTAMRI/MRAfMRI

Local increase in cerebral blood flow and volume after stimulation of eloquent cortex

Diffusion-Tensor ImagingVisualization of white matter pathways and their relationship to AVM

Imaging

Imaging

Pretherapeutic Evaluation

Invasive TechniquesProvocative Injection Testing(Wada’s Test)

Amobarbital sodium injection of selective feeding vessels to predict/avoid post-embolization deficits

Pretherapeutic Evaluation

AngiographyArterial feeders, size of AVM, nidus characteristics, drainage patternOther anatomical characteristics

deep location, deep venous drainage pattern, presence of a single draining vein, venous stenosis, eloquent location and diameter of AVM

Associated aneursyms(feeding artery, intranidal, circle of Willis, venous)PseudoaneurysmsAVM-associated AV Fistulas

Pretherapeutic Evaluation

AngiographyAngiogram following hemorrhage can result in false negative secondary to nidus compressionGold standard is follow-up angiogram 3 months after hemorrhage for detection of AVM

Perioperative/Anesthetic Considerations

Continuous arterial transductionsDeliberate systemic hypotensionGeneral anesthesiaadenosine-induced cardiac pause – slow flow through AVM for controlled deposition of embolic material

Pulse Oximeter Ipsilateral to femoral sheathVessel obstruction, thromboemboli, over-compression following sheath removal

Foley catheter- fluid management(Supplemental O2 // Nasopharyngeal airways for those under sedative-hypnotic agent)

Anatomy-Based Management

Neuroanatomy to understand at-risk territoriesDone under general anesthesia

Patient comfortEnsures motionless patient

Theoretically, because AVM has no functional intervening tissue, embolization of appropriate vessels should not cause functional deficitNeurophysiologic monitoring

SSEP/EEG

Physiology-Based Management

Evaluation of functional anatomy during procedureRequires intravenous anesthesia with short-acting agents(propofol, midazolam)Wide variability and cortical reorganization described in AVM patients

Endovascular Technique

Preoperative discussionVascular access with No. 7 Fr gauge sheath into femoral artery via Seldinger techniqueAnticoagulation algorithms to prevent thromboembolic complications

JHN-continuous heparinized flush, no bolusNo. 6 Fr gauge guiding catheter introduced into ICA or verterbral arteryFlow-directed/flow-assisted microcatheters to reach intranidal target

Variability in flexibility, torque, maneuverability, and responsiveness.

Identification of Embolization Point

Tip of catheter directly into nidusTip of catheter into feeder that does not share supply with adjacent normal brain

If normal brain at risk, pretherapeutic/intraoperative functional evaluation can be performed to avoid neurologic deficit from embolization

Injection of Embolic Material

Polyvinyl alcoholn-butyl cyanoacrylateOnyxEthiblocSilkMicrocoilsCombination

Polyvinyl Alcohol (PVA)

Available in different sizes based on size of target vesselsSlower occlusion than liquid embolic agentsOcclude low-pressure shunts first

Results in increase in intranidal vessel pressure hemorrhage risk prior to nidal obliteration

High recanalization ratesDevelopment of collateral feeders secondary to proximal occlusion of AVM with large size particles may contribute to this high rate

Used with success preoperatively to reduce flow prior to open or radiosurgical treatment

n-BCA

Liquid monomer that permanently polymerizes to a solid compound after contact with anionsOcclusion by initiation of inflammatory endothelial responseCombined with Ethiodal (iodine-based oil) to make lesion opaque on X-rays

Tantalum powder added to increase opacity(currently less common)

n-BCA

Viscosity and Polymerization timeIncreasing Ethiodal concentration increases viscosity and delays polymerization

Delayed polymerization helpful in lesions that exhibit slow flowIncreased viscosity delays transit within lesion

Temperature, homogeneity of mixture, and changes in pH of solution also influence polymerization time

n-BCA

Acetic acid and glaciar acid to decrease pHDelays polymerization without compromising viscosity

Dextrose 5%Delays polymerization time by delaying contact of blood with n-BCA

n-BCA

Factors that influence choice of viscosity and polymerization time:

Distance between microcatheter and nidusTortuosity of vesselsIntranidal flow

n-BCA

1:1 dilution(nBCA:oil) used when flow is very fast and catheter is close to nidus

n-BCA

“Flow Control” – Microcatheter occludes distal blood flow as it reaches smaller vessels, thus preventing blood from contacting glue, allowing for distal penetrationInjection stops when glue reaches venous system through nidus or there is backflow towards the catheterRemove catheter quickly to prevent catheter retention

Onyx

Ethylene-vinyl alcohol copolymer(EVOH) mixed in dimethyl-sulfoxide(DMSO) solventTantalum for radiopacityLower concentrations of EVOH decreased viscositySoft and nonadhesive mass that does not fragment

Increased embolization from single catheter positionAllows for angiography between injections

Nonabsorbable permanent occlusion

Onyx

PitfallsAngiotoxicity related to DMSO

swine rete mirabilis embolization model report risk of mild transient acute vasospasm

Separation of tantalum from OnyxIncreases difficulty of viewing smaller feeding pedicles

Treatment Objectives

Embolization for definitive cureEmbolization as a precursor for definitive operative resectionEmbolization as a precursor for radiosurgeryEmbolization as palliative treatment for progressive debilitating symptomsTarget embolization of high risk lesions

Treatment Objectives

Embolization for definitive cureN-BCA complete obliteration rates(~10%)

Deruty, et al – 5% but primarily used in high-grade AVMVinuela, et al – 9.9% in small to medium AVM with less than 4 pedicles(405 pts)Lundqvist, et al – 13% Valavanis and Yasargil – 40% in 387 consecutive patientsGobin – 11.2% in patients after embolization prior to radiosurgery (125 pts who were poor surgical candidates)

Treatment Objectives

Embolization for definitive cureOnyx complete obliteration rates

Perez-Higueras, et al – 22% in series of 45 patientsPierot, et al – 4.2% in series of 48 patientsLeonardi, et al – 5.9% among 34 pts SM III-IVvan Rooij, et al – 15.9% among 44 pts SM I-IIWeber, et al – 20% among 93 patientsMounayer, et al – 27.7% among 94 patients treated with Onyx, n-BCA, or combinationPanagiotopoulos – 24.4% among 82 pts

Reconstitution of flow to AVM nidus can occur through dilation of pre-existent collateralization

Rare cases reported for n-BCARecent reports of reperfusion for Onyx(Perez-Higuera, Weber, Panagiotopoulos)

Treatment Objectives

Anatomic features predictive of angiographic cure with n-BCA (Valavanis and Christoforidis)

Direct or dominant feeding arteriesMonocompartmental nidusDominant fistulous component of nidus without perinidal angiogenesis

Anatomic features predictive of angiographic cure with Onyx

Supratentorial and cortical locationCompact and plexiform nidusSmall number of supplying(direct) feeders1 superficial draining vein

Case 1

26 yo female PMH migraines who presented with a seizure two years ago. Imaging revealed R temporoparietal AVM fed by MCA and PCA branches, with superficial drainage veins

Case 1

Patient underwent staged embolization with n-BCA over three sessions to achieve angiographic obliteration of AVM

Treatement Objectives

Embolization as a precursor for definitive operative resection

Goals:Reduction of size of nidusOcclusion of deep arterial feeding vessels which may be surgically inaccessibleTreatment of intranidal aneurysms and high-flow fistulas to promote progressive nidus thrombosisReduce blood loss, improve operative time, convert high Spetzler-Martin AVMs to lower grade lesions reduce morbidity and mortality

Treatment Objectives

Embolization as a precursor for definitive operative resection

Avoid embolizing draining veinsRestricting venous outflow increases hemorrhage risk

Proximal embolization collateral development treacherous open surgical resection

Case 2

32 yo male with no PMH presented with seizure. Imaging revealed R temporal AVM being fed by the MCA with superficial drainage.

Embolization of M4 pedicle and Anterior Temporal pedicle resulted in 95% treatment of AVM.

Craniotomy for complete excision of remaining AVM was performed.Intraoperatively, lesions embolized with n-BCA exhibit a harder, less compliant mass in contrast to lesions embolized with Onyx, which is a softer agent

Treatment Objectives

Embolization as a precursor for radiosurgeryGoals:

Decrease target size of AVMAllows higher dose of radiation to smaller volume

Reduce weakness in AVM angioarchitecture by eliminating intranidal/venous aneursyms

Reduces hemorrhage risk in latency period

Flow reduction alone without reduction in AVM volume does not improve radiosurgical success

Case 3

40 x 40 mm L parietal AVM fed by L MCA and PCA

Staged embolization over four sessions with n-BCA enabled reduction of AVM volume prior to radiosurgery. Patient now undergoing LINAC treatmetn for residual AVM.

Note residual AVM with diffuse pattern and persistence of early venous drainage

Treatment Objectives

Embolization as palliation for progressive debilitating symptoms

Alternative for large, non-resectable AVMsProgressive neurologic deficits secondary to arterial stealMedically intractible seizuresVenous hypertension causing HA or local mass effect from engorged veins

Target embolization of high-risk lesionsAssociated aneursymsIncreased pressure in veins that have outflow restriction

Rapidly forming collaterals reduces long-term effectiveness

Complications

Hemorrhage/EdemaArterial perforation, intranidal aneurysm rupture, draining vein occlusionOcclusive Hyperemia—passive engorgement of vessels and arterial stagnation in adjacent brain following obliteration of AVM resulting in edema/hemorrhageNormal Perfusion Pressure Breakthrough Theory—loss of autoregulation in surrounding ischemic tissue following embolization, resulting in disruption of capillary bedsMural necrosis induced by embolic material

Complications

Treatment of HemorrhageProtamine for reversal of anticoagulation

Treatment of EdemaSteroids

Complications

IschemiaInadvertent embolization of normal blood vesselsThrombotic emboliRetention of microcatheter

TreatmentDeliberate hypertensionPlatelet glycoprotein IIb/IIIa inhibitors

Morbidity and Mortality

10% morbidity regarding temporary neurological deficit8% morbidity regarding permanent deficit~1% mortalityComplications tend to occur in higher grade AVMs

Risk of Embolization by SM Grade—Kim, et al Neurosurgery 2006

Retrospective review of 153 patients, 508 vessels, 203 sessionsAge, sex, AVM grade, location of lesion, number and location of embolized arteries, and number of embolization sessions reviewed with respect to neurologic/vascular complicationsNumber of branches embolized was only variable related to neurologic deficit (p=0.017)

Risk of Embolization—Kim, et al Neurosurgery 2006

Immediate/Long term neurologic deficit(selection bias-most ii-iii not usually embolized; represent more challenging subset of lesions requiring multimodality tx)

Number of avm per grade was too small for meaningful analysis

Spetzler-Martin Grade

Immediate neurologic deficit (p=0.103)

Follow-up neurologic deficit

I 0 % 0 %

II 8 % 5%

III 12 % 7 %

IV 15 % 10%

V 18 % 18%

Conclusion

Pre-operative evaluationNoninvasive/Invasive ImagingAnesthetic/Perioperative ConsiderationsEndovascular TechniqueEmbolization MaterialsTreatment Objectives of Endovascular ApproachOutcomes/ComplicationsFuture

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